Activity and Circadian Rhythm of Sepsis Patients in the Intensive Care Unit

Early mobilization of critically ill patients in the Intensive Care Unit (ICU) can prevent adverse outcomes such as delirium and post-discharge physical impairment. To date, no studies have characterized activity of sepsis patients in the ICU using granular actigraphy data. This study characterizes the activity of sepsis patients in the ICU to aid in future mobility interventions. We have compared the actigraphy features of 24 patients in four groups: Chronic Critical Illness (CCI) sepsis patients in the ICU, Rapid Recovery (RR) sepsis patients in the ICU, non-sepsis ICU patients (control-ICU), and healthy subjects. We used several statistical and circadian rhythm features extracted from the patients' actigraphy data collected over a five-day period. Our results show that the four groups are significantly different in terms of activity features. In addition, we observed that the CCI and control-ICU patients show less regularity in their circadian rhythm compared to the RR patients. These results show the potential of using actigraphy data for guiding mobilization practices, classifying sepsis recovery subtype, as well as for tracking patients' recovery.Comment: 4 pages, IEEE Biomedical and Health Informatics (BHI) 201

Overlapping but disparate inflammatory and immunosuppressive responses to SARS-CoV-2 and bacterial sepsis: An immunological time course analysis

Both severe SARS-CoV-2 infections and bacterial sepsis exhibit an immunological dyscrasia and propensity for secondary infections. The nature of the immunological dyscrasias for these differing etiologies and their time course remain unclear. In this study, thirty hospitalized patients with SARS-CoV-2 infection were compared with ten critically ill patients with bacterial sepsis over 21 days, as well as ten healthy control subjects. Blood was sampled between days 1 and 21 after admission for targeted plasma biomarker analysis, cellular phenotyping, and leukocyte functional analysi

Immunotherapies for COVID-19: lessons learned from sepsis.

Therapeutic approaches to mitigate the severe acute lung injury associated with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection have rapidly entered clinical trials primarily on anecdotal observations and few clinical studies. Along with the clinical symptoms related to viral invasion, the reported molecular response known as the cytokine storm has attracted the greatest attention, in both the scientific and the lay press, as a cause of organ injury. [...

The impact of sarcopenia and acute muscle mass loss on long‐term outcomes in critically ill patients with intra‐abdominal sepsis

Abstract Background Sarcopenia is a known risk factor for poor outcomes across many chronic diseases. The impact on outcomes of both pre‐existing sarcopenia and acute muscle wasting (AMW) in acute critical illness caused by sepsis remain unclear. Methods We conducted a prospective longitudinal cohort study of critically ill patients with intra‐abdominal sepsis utilizing abdominal computed tomography at sepsis onset to determine baseline skeletal muscle index (SMI). Biomarkers of inflammation and catabolism were measured through 28 days while hospitalized. We performed follow‐up evaluations of strength and physical function at 3, 6, and 12 months, with interval CT analyses at 3 and 12 months to evaluate changes in muscle mass. Measured clinical outcomes included development of chronic critical illness (≥14 days in intensive care with persistent organ dysfunction), long‐term functional status, and 1 year mortality. Results Among 47 sepsis patients enrolled (mean age 53 ± 14 years), half (n = 23; 49%) were sarcopenic at baseline. Overall, sepsis patients exhibited acute and persistent muscle wasting with an average 8% decrease in SMI from baseline at 3 months (P = 0.0008). Sarcopenic (SAR) and non‐sarcopenic (NSAR) groups were similar in regards to age and comorbidity burden. SAR patients had greater acute physiologic derangement (APACHE II, 18 vs. 12.5), higher incidence of multiple organ failure (57% vs. 17%), longer hospital (21 vs. 12 days) and intensive care unit length of stays (13 vs. 4 days), and higher inpatient mortality (17% vs. 0%; all P < 0.05). Pre‐existing SAR was a strong independent predictor of early death or developing chronic critical illness (odds ratio 11.87, 95% confidence interval CI 1.88–74.9; P = 0.009, area under the curve 0.880) and was associated with significantly higher risk of 1‐year mortality (34.9% vs. 4.2%, p = 0.007). Lower baseline SMI was also predictive of poor functional status at 12 months (OR 0.89, 95% confidence interval 0.80–0.99; p = 0.039, area under the curve 0.867). Additionally, SAR patients had AMW with persistent muscle mass loss at 3 months that was associated with decreased health‐related quality of life and SF‐36 physical function domains (P < 0.05). Persistent AMW at 3 months was not predictive of mortality or poor functional status, with return to near‐baseline muscle mass among sepsis survivors by 6 months. Conclusions Critically ill patients have an acute and persistent loss of muscle mass after intra‐abdominal sepsis, which is associated with decreased health‐related quality of life and physical function at 3 months. However, pre‐existing sarcopenia, rather than persistent acute muscle mass loss at 3 months after sepsis, is independently associated with poor long‐term functional status and increased 1 year mortality

Chronic Critical Illness and the Persistent Inflammation, Immunosuppression, and Catabolism Syndrome

Dysregulated host immune responses to infection often occur, leading to sepsis, multiple organ failure, and death. Some patients rapidly recover from sepsis, but many develop chronic critical illness (CCI), a debilitating condition that impacts functional outcomes and long-term survival. The “Persistent Inflammation, Immunosuppression, and Catabolism Syndrome” (PICS) has been postulated as the underlying pathophysiology of CCI. We propose that PICS is initiated by an early genomic and cytokine storm in response to microbial invasion during the early phase of sepsis. However, once source control, antimicrobial coverage, and supportive therapies have been initiated, we propose that the persistent inflammation in patients developing CCI is a result of ongoing endogenous alarmin release from damaged organs and loss of muscle mass. This ongoing alarmin and danger-associated molecular pattern signaling causes chronic inflammation and a shift in bone marrow stem cell production toward myeloid cells, contributing to chronic anemia and lymphopenia. We propose that therapeutic interventions must target the chronic organ injury and lean tissue wasting that contribute to the release of endogenous alarmins and the expansion and deposition of myeloid progenitors that are responsible for the propagation and persistence of CCI

Additional file 1 of Defining critical illness using immunological endotypes in patients with and without sepsis: a cohort study

Additional file 1. Supplemental Materials: Methods